• Alopecia: absence of hair from areas where it normally grows
    • Anagen phase: growing hairs, 90% scalp hair follicles at any time, lasts 2 to 6 years
    • Catagen phase: regression of follicle, <1% follicles, lasts 3 weeks
    • Telogen phase: Resting phase lasts 2 to 3 months, 50 to 150 telogen hairs shed per day.
  • Classified as scarring (cicatricial), nonscarring (noncicatricial), or structural
  • Scarring (cicatricial) alopecia
    • Inflammatory disorders leading to permanent hair loss and follicle destruction
    • Includes lichen planopilaris, frontal fibrosing alopecia, and discoid lupus erythematosus
  • Nonscarring (noncicatricial) alopecia
    • Lack of inflammation, no destruction of follicle
    • Includes androgenic alopecia, alopecia areata (AA), telogen effluvium, anagen effluvium
  • Structural hair disorders
    • Brittle or fragile hair from abnormal hair formation or external insult



  • Androgenic alopecia:
    • In males, 30% Caucasian by 30 years of age, 50% by 50 years of age, and 80% by 70 years of age
    • In females, 70% of women >65 years of age
  • AA: 1/1,000 with lifetime risk of 1–2%, men and women affected equally
  • Scarring alopecia: rare, 3–7% of all hair disorder patients

Etiology and Pathophysiology

  • Scarring (cicatricial) alopecia
    • Inflammatory disorders leading to permanent destruction of the follicle
    • Slick smooth scalp without follicles evident
    • Three major subtypes based on type of inflammation: lymphocytic, neutrophilic, and mixed
    • Primary scarring includes discoid lupus, lichen planopilaris, dissecting cellulitis of scalp, primary fibrosing, among others.
    • Secondary scarring from infection, neoplasm, radiation, surgery, and other physical trauma, including tinea capitis
    • Central centrifugal cicatricial alopecia most common form of scarring hair loss in African American women; etiology unknown but likely secondary to hair care practices
  • Nonscarring (noncicatricial) alopecia
    • Focal alopecia
    • AA
      • Patchy hair loss, usually autoimmune in etiology, T cell–mediated inflammation resulting in premature transition to catagen then telogen phases
      • May occur with hair loss in other areas of the body (alopecia totalis [entire scalp]), alopecia universalis (rapid loss of all body hair)
      • Nail disease frequently seen
      • High psychiatric comorbidity (1)
    • Alopecia syphilitica: “moth-eaten” appearance, secondary syphilis
    • Postoperative, pressure-induced alopecia: from long periods of pressure on one area of scalp
    • Temporal triangular alopecia: congenital patch of hair loss in temporal area, unilateral or bilateral
    • Traction alopecia: patchy, due to physical stressor of braids, ponytails, hair weaves
  • Pattern hair loss
    • Androgenic alopecia: hair transitions from terminal to vellus hairs
    • Male pattern hair loss: androgen-mediated hair loss in specific distribution; bitemporal, vertex occurs where androgen sensitive hairs are located on scalp. This is a predominantly hereditary condition (2).
      • Increased androgen receptors, increased 5-α reductase leads to increased testosterone conversion in follicle to dihydrotestosterone (DHT). This leads to decreased follicle size and vellus hair (2).
      • Norwood Hamilton classification type I to VII
      • Female pattern hair loss: thinning on frontal and vertex areas (Ludwig classification, grade I to III). Females with low levels of aromatase have more testosterone available for conversion to DHT (3). This carries an unclear inheritance pattern (2).
      • Polycystic ovarian syndrome, adrenal hyperplasia, and pituitary hyperplasia all lead to androgen changes and can result in alopecia.
    • Medications (hormone replacement therapy, oral contraceptive pills)
    • Drugs (testosterone, progesterone, danazol, adrenocorticosteroids, anabolic steroids)
  • Trichotillomania: intentional pulling of hair from scalp; may present in variety of patterns
  • Diffuse alopecia
    • Telogen effluvium: sudden shift of many follicles from anagen to telogen phase resulting in decreased hair density but not bald areas
      • May follow major stressors, including childbirth, injury, illness; occurs 2 to 3 months after event
      • Can be chronic with ongoing illness, including SLE, renal failure, IBS, HIV, thyroid disease, pituitary dysfunction
      • Adding or changing medications (oral contraceptives, anticoagulants, anticonvulsants, SSRIs, retinoids, β-blockers, ACE inhibitors, colchicine, cholesterol-lowering medications, etc.)
      • Malnutrition from malabsorption, eating disorders; poor diet can contribute.
    • Anagen effluvium
      • Interruption of the anagen phase without transition to telogen phase; days to weeks after inciting event
      • Chemotherapy is most common trigger.
      • Radiation, poisoning, and medications can also trigger.
  • Structural hair disorders
    • Multiple inherited hair disorders including Menkes disease, monilethrix, and so forth. These result in the formation of abnormal hairs that are weakened.
    • May also result from chemical or heat damaging from hair processing treatments

Family history of early patterned hair loss is common in androgenic alopecia, also in AA.

Risk Factors

  • Genetic predisposition
  • Chronic illness including autoimmune disease, infections, cancer
  • Physiologic stress including pregnancy and childbirth
  • Poor nutrition
  • Medication, chemotherapy, radiation
  • Hair chemical treatments, braids, weaves/extensions

General Prevention

Minimize risk factors where possible.

Commonly Associated Conditions

  • See “Etiology and Pathophysiology.”
  • Vitiligo—4.1% patients with AA, may be the result of similar autoimmune pathways (4)

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